Insulin receptors and responsiveness have been studied in undifferentiated and fatty 3T3-L1 fibroblasts. With differentiation, 3T3-L1 fibroblasts develop lipoprotein lipase. Insulin and insulin receptor antibody stimulate release of lipase from the cells as well as increase intracellular lipoprotein lipase activity. Glucocorticoid hormones induce insulin resistance in 3T3-L1 cells. The affinity of the receptor for insulin is decreased and there is inhibition of the insulin response at a post-receptor site. With differentiation, 3T3-L1 cells develop surface markings characteristic of fat cells. Insulin is taken up into the cell by a pathway utilizing coated pits.